State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, China.
Hubei Key Laboratory of Plant Pathology, College of Plant Science and Technology, Huazhong Agricultural University, Wuhan, China.
BMC Biol. 2024 Oct 21;22(1):239. doi: 10.1186/s12915-024-02043-4.
Botrytis cinerea is a broad-host-range pathogen causing gray mold disease and significant yield losses of numerous crops. However, the mechanisms underlying its rapid invasion and efficient killing of plant cells remain unclear.
In this study, we elucidated the dynamics of B. cinerea infection in Arabidopsis thaliana by live cell imaging and dual RNA sequencing. We found extensive transcriptional reprogramming events in both the pathogen and the host, which involved metabolic pathways, signaling cascades, and transcriptional regulation. For the pathogen, we identified 591 candidate effector proteins (CEPs) and comprehensively analyzed their co-expression, sequence similarity, and structural conservation. The results revealed temporal co-regulation patterns of these CEPs, indicating coordinated deployment of effectors during B. cinerea infection. Through functional screening of 48 selected CEPs in Nicotiana benthamiana, we identified 11 cell death-inducing proteins (CDIPs) in B. cinerea.
The findings provide important insights into the transcriptional dynamics and effector biology driving B. cinerea pathogenesis. The rapid infection of this pathogen involves the temporal co-regulation of CEPs and the prominent role of CDIPs in host cell death. This work highlights significant changes in gene expression associated with gray mold disease, underscoring the importance of a diverse repertoire of effectors crucial for successful infection.
灰葡萄孢是一种广泛宿主范围的病原体，可引起灰霉病，并导致许多作物的产量显著损失。然而，其快速入侵和有效杀死植物细胞的机制仍不清楚。
在这项研究中，我们通过活细胞成像和双 RNA 测序阐明了灰葡萄孢在拟南芥中的感染动态。我们发现病原体和宿主都发生了广泛的转录重编程事件，涉及代谢途径、信号级联和转录调控。对于病原体，我们鉴定了 591 个候选效应蛋白 (CEP)，并全面分析了它们的共表达、序列相似性和结构保守性。结果揭示了这些 CEP 的时间协同调控模式，表明在灰葡萄孢感染过程中协调部署效应蛋白。通过在本氏烟中对 48 个选定的 CEP 进行功能筛选，我们鉴定了灰葡萄孢中的 11 个细胞死亡诱导蛋白 (CDIP)。
这些发现为驱动灰葡萄孢发病机制的转录动态和效应物生物学提供了重要的见解。该病原体的快速感染涉及 CEP 的时间协同调控以及 CDIP 在宿主细胞死亡中的突出作用。这项工作突出了与灰霉病相关的基因表达的显著变化，强调了成功感染所需的多样化效应物库的重要性。
